Ulcerative endocarditis may produce a sudden incompetency of the valve, with great and perhaps fatal embarrassment of the cardiac circulation, as already mentioned. And, finally, sudden mus cular strain may produce a rupture of one of the segments, especially if the valve is previously impaired by disease. Pathology.—Besides the usual changes in the valves themselves, there are lesions peculiar to aortic regurgitation in the heart and blood-vessels. As already stated, the heart becomes enormously hypertrophied, weighing 40 to 45 ounces instead of 10 or 12. The main part of this increase is in the walls of the left ventricle, the cavity of which is enlarged, hut its walls more than proportionately thickened. The muscular trabecuhe of the ventricle are usually more or less flattened where the regurgitant blood current impinges upon them.
While in all kinds of valvular lesions the heart is exposed to ultimate degen erative changes, this liability is particu larly great in aortic regurgitation, be cause the coronary arteries upon which the nutrition of the heart-wall depends, originating, as they do, at the base of the semilunar valves, no longer have a normal amount of blood forced into them. Moreover, if the lesion of the valves is due to fibrotic changes, the orifices of the coronary arteries are apt to be in volved in this process and more or less occluded. Hence those cases of aortic regurgitation have a decidedly better prognosis which are due to rheumatism than those which are associated with at h erom a .
The systemic arteries become dilated by the large volume of blood which is thrown into them with each contraction of the enormous left ventricle, and they also undergo sclerotic degeneration be cause of the strain which they experience.
Prognosis.—Aortic regurgitation is the most dangerous of the acquired valvu lar lesions of the heart. It is consistent with comfort and vigor lasting for years, but there is always the possibility of a sudden fatal termination; and, when once compensation has been interrupted, it is seldom satisfactorily restored. Some times upon the development of secondary mitral insufficiency there will be a no ticeable alleviation of the cardiac embar rassment, but the patient is reprieved, not saved.
Sudden death in heart disease occurs in about one-quarter of the cases of aortic regurgitation. Thirty fatal eases of valvular disease have been personally observed with the average age of death for mitral stenosis at 50, for mitral in sufficiency at 40, and for mitral stenosis and insufficiency at 36. In 250 cases of which records have been kept, its aver age duration in mitral insufficiency was found to be 5.1 years, in mitral stenosis, 11.5 years, in aortic stenosis, 7 years, and
in aortic insufficiency 2.3 years. The maximum duration was 17 years in mi tral insufficiency, and in aortic stenosis 20 years. In aortic insufficiency it was only 4 years. The prognosis is also governed, to a certain extent, by the heart-sounds, a vigorous murmur, and first sound, being favorable. Congenital lesions usually do better than those that have been acquired. If the heart is greatly hypertrophied, the prognosis is less favorable. If there is anmmia or emaciation, or if there is a sudden obesity, the case is graver. The dura tion of broken compensation is very variable. In mitral insufficiency it aver ages 2.6 years; in stenosis, 3.6 years; in aortic stenosis, 3.8; in aortic insuffi ciency, 2.75 years. Unfavorable symp toms in lost compensation are arimia, dropsy, and dilatation of the heart; but, when it occurs, the patients are usually more amenable to hygienic measures. In 139 cases of the 250 no satisfactory cause could be determined. In the re maining cases 54 were due to rheuma tism, 15 to atheroma, 5 to chorea, and the others apparently to infectious dis ease. N. S. Davis, Jr. (Med. News, June 17, '99).
Treatment. — When the aortic valves are diseased from causes other than endo carditis, iodide of potash in doses of 5 to 10 grains thrice daily should be given for long periods. This applies to cases of stenosis as well as regurgitation. Some writers have advised against the use of digitalis in aortic insufficiency, fearing the bad effect of lengthening the diastole and thus affording a longer time for regurgitation; but the weight of authority is undoubtedly in favor of employing digitalis when it seems to be needed, despite this theoretical objection. Further suggestions will be found in the article in the previous volume on DILATATION OF THE HEART, and in gen eral remarks upon the treatment of val vular diseases, below.
Aortic Stenosis.
Definition. — A lesion of the aortic valve obstructing the normal flow of blood from the left ventricle into the aorta.
Symptoms. — Well-compensated aortic stenosis may last for years without sub jective disturbances. When compensa tion begins to fail, the pulse may become very slow, even as slow as 50 to 25 beats a minute, and there is a great tendency to dizziness, faintness, syncope, and epi leptiform attacks. The subjects of the disease are usually elderly persons with general arterial sclerosis. Upon inspec tion, the heart's apex may be seen down ward and to the left from its normal posi tion; but in some instances, when there is pulmonary emphysema or an unyield ing chest-wall, no cardiac impulse can be seen or even felt.